Heart failure is a debilitating disease in which abnormal function of the heart leads in the direction of inadequate blood flow to fulfill the needs of the tissues and organs of the body. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately eject or fill with blood between heartbeats and the valves regulating blood flow become leaky, allowing regurgitation or back-flow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness and the inability to carry out daily tasks may result. Not all heart failure patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive. As heart failure progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds muscle causing the ventricles (particularly the left ventricle) to grow in volume in an attempt to pump more blood with each heartbeat. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output. A particularly severe form of heart failure is congestive heart failure (CHF) wherein the weak pumping of the heart leads to build-up of fluids in the lungs and other organs and tissues.
The current standard treatment for heart failure is typically centered on medical treatment using angiotensin converting enzyme (ACE) inhibitors, diuretics, beta-blockade, and digitalis. Cardiac resynchronization therapy (CRT) may also be employed, if a biventricular pacing device is implanted. Briefly, CRT seeks to normalize asynchronous cardiac electrical activation and resultant asynchronous contractions associated with CHF by delivering synchronized pacing stimulus to both ventricles. The stimulus is synchronized so as to improve overall cardiac function. This may have the additional beneficial effect of reducing the susceptibility to life-threatening tachyarrhythmias. CRT and related therapies are discussed in, for example, U.S. Pat. No. 6,643,546 to Mathis, et al. entitled “Multi-Electrode Apparatus and Method for Treatment of Congestive Heart Failure”; U.S. Pat. No. 6,628,988 to Kramer, et al., entitled “Apparatus and Method for Reversal of Myocardial Remodeling with Electrical Stimulation”; and U.S. Pat. No. 6,512,952 to Stahmann, et al., entitled “Method and Apparatus for Maintaining Synchronized Pacing”.
In view of the potential severity of heart failure, it is highly desirable to track the progression of the condition so that appropriate therapy can be provided. Many patients suffering heart failure already have pacemakers or ICDs implanted therein or are candidates for such devices. Accordingly, it is desirable to provide such devices with the capability to automatically track progression of heart failure. Some aspects of the present invention are directed to this end.
Pulmonary edema is a swelling and/or fluid accumulation in the lungs often caused by heart failure (i.e. the edema represents one of the “congestives” of CHF.) Briefly, the poor cardiac function resulting from heart failure can cause blood to back up in the lungs, thereby increasing blood pressure in the lungs, particularly pulmonary venous pressure. The increased pressure pushes fluid—but not blood cells—out of the blood vessels and into lung tissue and air sacs (i.e. the alveoli). This can cause severe respiratory problems and, left untreated, can be fatal. Pulmonary edema can also arise due to other factors besides heart failure, such as infections.
One therapy delivered to address pulmonary edema is to administer diuretics to the patient in an effort to reduce the amount of fluids within the thorax of the patient. One technique uses thoracic electrical impedance measurements to detect a “fluid overload,” i.e. a significant increase in thoracic fluids. A drop in thoracic impedance is deemed to be indicative of such a fluid overload. In response, diuretics such as furosemide or bumetanide are administered to the patient to reduce the fluid overload. (Diuretics are drugs that increase the flow of urine, thus eliminating water from the body, ultimately reducing thoracic fluid levels.)
The use of electrical impedance is promising since thoracic impedance can be readily measured in situ using pacemaker or ICDs. However, a significant concern with thoracic impedance-based techniques is that the thoracic impedance measurement provides only a relative measurement of thoracic fluid levels, i.e. the technique merely detects a drop in impedance indicative of a possible increase in thoracic fluid levels. It does not necessarily establish that thoracic fluid levels have increased beyond an acceptable range. Moreover, impedance drops can occur frequently within some patients without any clinical consequences and are often merely “false positive” events. When titrating a patient with diuretics based on such drops in thoracic impedance, it is thus possible to overcorrect the fluid overload by dispensing too much diuretic. The patient may then become hypovolemic (a condition wherein there is too little blood).
Accordingly, it would also be desirable to provide improved techniques for monitoring thoracic fluid levels, which avoid the aforementioned problems, and it is to this end that aspects of the invention are primarily directed. It is particularly desirable to provide techniques for titrating diuretics within patients to keep thoracic fluid levels within an optimal range and such techniques are described herein.